Institute of Bioimaging and Molecular Physiology, CNR, Segrate (Milano), Italy.
Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milano, Italy.
PLoS One. 2014 Jan 31;9(1):e87506. doi: 10.1371/journal.pone.0087506. eCollection 2014.
Beneficial systemic effects of regular physical exercise have been demonstrated to reduce risks of a number of age-related disorders. Antioxidant capacity adaptations are amongst these fundamental changes in response to exercise training. However, it has been claimed that acute physical exercise performed at high intensity (>60% of maximal oxygen uptake) may result in oxidative stress, due to reactive oxygen species being generated excessively by enhanced oxygen consumption. The aim of this study was to evaluate the effect of high-intensity discontinuous training (HIDT), characterized by repeated variations of intensity and changes of redox potential, on oxidative damage. Twenty long-distance masters runners (age 47.8 ± 7.8 yr) on the basis of the individual values of gas exchange threshold were assigned to a different 8-weeks training program: continuous moderate-intensity training (MOD, n = 10) or HIDT (n = 10). In both groups before (PRE) and after (POST) training we examined the following oxidative damage markers: thiobarbituric acid reactive substances (TBARS) as marker of lipid peroxidation; protein carbonyls (PC) as marker of protein oxidation; 8-hydroxy-2-deoxy-guanosine (8-OH-dG) as a biomarker of DNA base modifications; and total antioxidant capacity (TAC) as indicator of the overall antioxidant system. Training induced a significant (p<0.05) decrease in resting plasma TBARS concentration in both MOD (7.53 ± 0.30 and 6.46 ± 0.27 µM, PRE and POST respectively) and HIDT (7.21 ± 0.32 and 5.85 ± 0.46 µM, PRE and POST respectively). Resting urinary 8-OH-dG levels were significantly decreased in both MOD (5.50 ± 0.66 and 4.16 ± 0.40 ng mg(-1)creatinine, PRE and POST respectively) and HIDT (4.52 ± 0.50 and 3.18 ± 0.34 ng mg(-1)creatinine, PRE and POST respectively). Training both in MOD and HIDT did not significantly modify plasma levels of PC. Resting plasma TAC was reduced in MOD while no significant changes were observed in HIDT. In conclusion, these results suggest that in masters runners high-intensity discontinuous does not cause higher level of exercise-induced oxidative stress than continuous moderate-intensity training, inducing similar beneficial effects on redox homeostasis.
定期进行体育锻炼对身体有诸多益处,已被证实可降低多种与年龄相关疾病的发病风险。抗氧化能力的适应性改变是运动训练产生的基本变化之一。然而,有人声称,高强度(>60%最大摄氧量)的急性运动可能会导致氧化应激,因为氧消耗增加会导致过多的活性氧生成。本研究的目的是评估高强度不连续训练(HIDT)对氧化损伤的影响,HIDT 的特点是强度反复变化和氧化还原电位变化。根据个体的气体交换阈值,将 20 名长跑大师(年龄 47.8±7.8 岁)分为不同的 8 周训练方案:持续中等强度训练(MOD,n=10)或 HIDT(n=10)。在训练前后(PRE 和 POST),我们检查了以下氧化损伤标志物:硫代巴比妥酸反应物质(TBARS)作为脂质过氧化的标志物;蛋白质羰基(PC)作为蛋白质氧化的标志物;8-羟基-2-脱氧鸟苷(8-OH-dG)作为 DNA 碱基修饰的生物标志物;总抗氧化能力(TAC)作为整体抗氧化系统的指标。训练使 MOD(7.53±0.30 和 6.46±0.27µM,分别为 PRE 和 POST)和 HIDT(7.21±0.32 和 5.85±0.46µM,分别为 PRE 和 POST)中静息血浆 TBARS 浓度显著降低(p<0.05)。MOD(5.50±0.66 和 4.16±0.40ngmg(-1)肌酸酐,分别为 PRE 和 POST)和 HIDT(4.52±0.50 和 3.18±0.34ngmg(-1)肌酸酐,分别为 PRE 和 POST)中静息尿 8-OH-dG 水平显著降低。MOD 训练时静息血浆 PC 水平没有显著改变,而 HIDT 训练时没有显著变化。MOD 训练时静息血浆 TAC 降低,而 HIDT 训练时没有观察到静息血浆 TAC 变化。综上所述,这些结果表明,在大师跑者中,高强度不连续运动不会引起比持续中等强度训练更高水平的运动诱导氧化应激,对氧化还原平衡产生类似的有益影响。